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Cellular and Molecular Mechanisms in Lung Health and Disease
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Cellular and Molecular Mechanisms in Lung Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 June 2025) | Viewed by 2990

Special Issue Editor

Dr. Verena Tretter

E-Mail Website
Guest Editor
Department of Anesthesia and General Intensive Care, Clinical Department of Anesthesia, Medizinische Universität Wien, Vienna, Austria
Interests: cell biology of the lung and heart; organ protection; signaling transduction in the lung; experimental anesthesiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The lung, as the central organ of the respiratory system, functions to exchange oxygen from the inhaled air for carbon dioxide, an asphyxiant waste product of the metabolism.

Due to this crucial function, diseases of the lung have a severe impact on the wellbeing and are frequently even life-threatening, requiring mechanical ventilation or extracorporeal membrane oxygenation (ECMO). Pathologies of the respiratory system can be grouped into airway disease (asthma, chronic obstructive pulmonary disease (COPD), bronchiolitis, etc.), tissue disease (fibrosis, inflammation, sarcoidosis, cancer, etc.), or circulation disease affecting the blood vessels (clotting, inflammation, etc.), triggered by inhalation of toxic substances, viral, bacterial, or fungal infections, or other organs’ malfunction. Severe pulmonary conditions, such as acute respiratory distress syndrome (ARDS), are frequently still difficult to treat; therefore, progress in the understanding of molecular mechanisms is demanded. Lung cells of epithelial, endothelial, stromal, or immune cell types were found to be very heterogenous by themselves. This fact complicates mechanistic studies, but methodology and analysis techniques also make rapid progress to tackle this challenge.

As the Guest Editor of this Special Issue, I would like to invite authors working in this field to contribute their original work, along with review articles, that enhance our understanding of the status quo of research on molecular mechanisms and cellular function in the healthy or diseased, preferably human, but also rodent, lung.

Dr. Verena Tretter
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lung disease
  • asthma, chronic obstructive pulmonary disease
  • fibrosis, inflammation, sarcoidosis

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Published Papers (3 papers)

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Research

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21 pages, 10060 KiB  
Article
The Effects of the Natriuretic Peptide System on Alveolar Epithelium in Heart Failure
by Yara Knany, Safa Kinaneh, Emad E. Khoury, Yaniv Zohar, Zaid Abassi and Zaher S. Azzam
Int. J. Mol. Sci. 2025, 26(7), 3374; https://doi.org/10.3390/ijms26073374 - 4 Apr 2025
Viewed by 565
Abstract
Alveolar active sodium transport is essential for clearing edema from airspaces, in a process known as alveolar fluid clearance (AFC). Although it has been reported that atrial natriuretic peptide (ANP) attenuates AFC, little is known about the underlying molecular effects of natriuretic peptides [...] Read more.
Alveolar active sodium transport is essential for clearing edema from airspaces, in a process known as alveolar fluid clearance (AFC). Although it has been reported that atrial natriuretic peptide (ANP) attenuates AFC, little is known about the underlying molecular effects of natriuretic peptides (NPs). Therefore, we examined the contribution of NPs to AFC and their effects as mediators of active sodium transport. By using the isolated liquid-filled lungs model, we investigated the effects of NPs on AFC. The expression of NPs, Na+, K+-ATPase, and Na+ channels was assessed in alveolar epithelial cells. Congestive heart failure (CHF) was induced by using the aortocaval fistula model. ANP and brain NP (BNP) significantly reduced AFC rate from 0.49 ± 0.02 mL/h in sham rats to 0.26 ± 0.013 and 0.19 ± 0.005 in ANP and BNP-treated groups, respectively. These effects were mediated by downregulating the active Na+ transport components in the alveolar epithelium while enhancing the ubiquitination and degradation of αENaC in the lungs, as reflected by increased levels of Nedd4-2. In addition, AFC was reduced in compensated CHF rats treated with ANP, while in decompensated CHF, ANP partially restored AFC. In conclusion, NPs regulate AFC in health and CHF. This research could help optimize pharmacological treatments for severe CHF. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Lung Health and Disease)
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23 pages, 4925 KiB  
Article
Characterizing SV40-hTERT Immortalized Human Lung Microvascular Endothelial Cells as Model System for Mechanical Stretch-Induced Lung Injury
by Beatrix Hochreiter, Claudia Lindner, Matthias Postl, Eva Hunyadi-Gulyas, Zsuzsanna Darula, Oliver Domenig, Smriti Sharma, Irene M. Lang, Attila Kiss, Andreas Spittler, Konrad Hoetzenecker, Roman Reindl-Schwaighofer, Katharina Krenn, Roman Ullrich, Matthias Wieser, Regina Grillari-Voglauer and Verena Tretter
Int. J. Mol. Sci. 2025, 26(2), 683; https://doi.org/10.3390/ijms26020683 - 15 Jan 2025
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Abstract
Drug development for human disease relies on preclinical model systems such as human cell cultures and animal experiments before therapeutic treatments can ultimately be tested on humans in clinical studies. We here describe the generation of a novel human cell line (HLMVEC/SVTERT289) that [...] Read more.
Drug development for human disease relies on preclinical model systems such as human cell cultures and animal experiments before therapeutic treatments can ultimately be tested on humans in clinical studies. We here describe the generation of a novel human cell line (HLMVEC/SVTERT289) that we generated by transfection of microvascular endothelial cells from healthy donor lung tissue with the catalytic domain of telomerase and the SV40 large T/small t-antigen. These cells exhibited satisfactory growth characteristics and largely maintained their native characteristics, including morphology, cell surface marker expression, angiogenic potential and the protein composition of secreted extracellular vesicles. In order to test their suitability as a disease model, we simulated mechanical stress induced by cyclic stretch as encountered in ventilator-induced lung injury using the FlexCell® system and compared their performance to primary lung endothelial cells. In this setting, HLMVEC/SVTERT289 cells exhibited significantly higher neprilysin activity on the cell surface and extracellular vesicles secreted from the cell line exhibited higher Tissue Factor and ACE2 expression but lower ACE expression and ACE activity than vesicles released from the primary cells. This study provides an unprecedented and detailed characterization of the HLMVEC/SVTERT289 cell line, which should help to appraise its suitability in different molecular studies. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Lung Health and Disease)
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Review

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13 pages, 702 KiB  
Review
Mitochondrial DNA Copy Numbers and Lung Cancer: A Systematic Review and Meta-Analysis
by Manuela Chiavarini, Jacopo Dolcini, Giorgio Firmani, Kasey J. M. Brennan, Andrès Cardenas, Andrea A. Baccarelli and Pamela Barbadoro
Int. J. Mol. Sci. 2025, 26(14), 6610; https://doi.org/10.3390/ijms26146610 - 10 Jul 2025
Viewed by 136
Abstract
LC continues to be the leading cause of cancer mortality globally, among both males and females, representing a major public health challenge. The impact of mitochondria on human health and disease is a rapidly growing focus in scientific research, due to their critical [...] Read more.
LC continues to be the leading cause of cancer mortality globally, among both males and females, representing a major public health challenge. The impact of mitochondria on human health and disease is a rapidly growing focus in scientific research, due to their critical roles in cellular survival and death. Mitochondria play an important role in controlling imperative cellular parameters, and alterations in mtDNAcn might be crucial for LC development. MtDNAcn has been studied as a possible marker for LC risk, but its role in prevention is still unclear. This review and meta-analysis aims to summarize the current evidence and provide an overall estimate of the relationship between the mtDNA copy number in human samples like blood and sputum. PubMed, Web of Science, and Scopus databases were used for studies published up to February 2024, following PRISMA and MOOSE guidelines. Studies were combined using a random-effects model, and we assessed the heterogeneity between studies with the chi-square-based Cochran’s Q statistic and the I2 statistic. Publication bias was checked using Begg’s and Egger’s tests. Five studies, including a total of 3.748 participants, met the eligibility criteria. The MtDNA copy number was measured in blood or sputum samples and compared across different quantiles. The pooled analysis did not find a significant association between the mtDNA copy number and LC risk (OR = 0.94; 95% CI: 0.49–1.78). Moreover, when looking at different study designs, no significant results were found, due to the small number of studies available. No significant publication bias was detected. Further studies are needed to better understand the connection between the mtDNA copy number and LC risk and to better understand the role of potential confounders. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Lung Health and Disease)
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